Femoroacetabular impingement (FAI) is characterized by abnormal bone growth on the femur and/or acetabulum in the hip and may be the principle etiology of hip osteoarthritis (OA). Patients diagnosed with FAI exhibit restricted hp joint motion and damaged cartilage and labral (i.e., chondrolabral) tissue, suggesting that FAI restricts range of motion and elevates chondrolabral stresses. Biomechanical factors are considered the key initiator of OA. Thus, to establish the link between FAI and OA, it is imperative to confirm that FAI patients indeed have deleterious hip biomechanics. Unfortunately, hip impingement has yet to be observed in-vivo. Furthermore, it is not understood whether muscle activations/forces and chondrolabral mechanics are disrupted in the hip with FAI. The goals of this fellowship are therefore to measure hip kinematics, muscle forces/activations, and chondrolabral stresses in live human subjects with and without FAI. For Aim 1, dual fluoroscopy and model-based markerless tracking will capture the motion of hip bones while subjects walk, squat and pivot, and reflective marker-based motion capture will track kinematics for those joints outside of the dual fluoroscopy field of view. Muscle models developed as part of Aim 1 will then predict muscle activations and forces required to produce the observed movements and will estimate the net hip joint reaction force (JRF). The hypothesis of Aim 1 is that, relative to controls, during walking, squatting and pivoting motions, patients with FAI will have reduced hip range of motion, different locations of minimum bone- to-bone distance/impingement, and altered muscle activation/force levels. For Aim 2, finite element (FE) models will predict tissue mechanics during the activities from Aim 1. FE models will include patient-specific bone and chondrolabral tissue anatomy and will be loaded using the hip JRF quantified from Aim 1. Using the FE-predicted chondrolabral tissue biomechanics, a validated stress-threshold-criterion will evaluate the risk of OA in hips with FAI. It is expected that FAI patients will experience increased maximum shear stress near the osteochondral and chondrolabral borders, and that areas of maximum stress will correspond to locations of damage observed intra-operatively for the same patients. The long-term goal of this work is to establish an empirical link between FAI and OA. Aim 1 will clarify if FAI patients move differently than size-matched controls (via joint kinematics), use their muscles differently (muscle activations/forces) and experience potentially damaging higher joint reaction forces. Aim 2 will show how differences in kinematics, forces and anatomy result in dissimilar (and deleterious) chondrolabral mechanics that may lead to OA later in life. Together, Aims 1 and 2 will result in the most comprehensive biomechanical study of FAI and help provide direction for future investigations of FAI and OA. The fellowship training program will encapsulate all aspects of experimental and computational biomechanics and will prepare the applicant for a successful career in musculoskeletal research.